All these three p53‐aberrant tumours showed very high degrees of DNA damage checkpoint activation (γH2AX marker and ATR/ATM pathways activation), consistent with the notion that DNA damage signalling activates p53 and one of the pathogenic routes to escape from such checkpoint pressure in order to progress towards full malignancy is selection of tumour cells with mutant p53 (Halazonetis et al., 2008). The gene discussed is ATR; the disease is neoplasm.